Studies on the pathogenesis of B cell malignancies

KHM-10B是从一名Burkitt淋巴瘤患者身上建立的。常规细胞遗传学分析未发现8q24参与，Southern杂交检测不到c-myc癌基因重排。然而，荧光原位杂交(FISH)检测到掩蔽的t(8；22)(q24；q11)是22q11的部分易位到了8q24。用羟基脲和硫胺嘧啶使KHM-10B细胞停滞在S期，并在无药物的培养液中同步化细胞进行细胞周期。与在另一个Burkitt淋巴瘤细胞系Raji中发现的一样，c-myc和max在整个细胞周期中都有结构性表达。KHM-11是从一位对长春新碱、阿霉素和地塞米松联合治疗(VAD)高度耐药的IgA-kappa型进行性骨髓瘤患者的胸腔积液中建立的。除表达正常浆细胞抗原CD38和Pca-1外，新鲜细胞和KHM-11细胞均表达CD45。其他T或B细胞抗原，如CD2、4、8、19和20均为阴性。KHM-11细胞培养上清液中存在IL-6，该上清液可刺激KHM-11细胞生长，提示IL-6的自分泌机制。这些结果表明KHM-11是一种CD45阳性的未成熟浆细胞系，KHM-10B和KHM-11这两种细胞系都可以作为了解B细胞恶性肿瘤发病机制的有用工具。

KHM-10B was established from a patient with Burkitt's lymphoma. Conventional cytogenetic analysis revealed no detectable 8q24 involvement, and the rearrangement of c-myc oncogene could not detected by Southern blot study. However, fluorecence in situ hybridization (FISH) assay identified masked t(8 ; 22)(q24 ; q11) which is the 22q11 portion was translocated to the 8q24 locus. Using hydroxyurea and thimidine, the KHM-10B cells were arrested at S phase, and the syncronized cells progressed the cell cycle in drug free medium. The constitutive expressions of c-myc and max were observed throughout the cell cycle ; as was found in another Burkitt's lymphoma cell line, Raji.KHM-11 was established from the pleural effusion of a patient with IgA-kappa type aggresive myeloma with high serum lactate dehydrogenase who was extermely resistant to vincristin, adriamycin and dexamethasone combination therapy (VAD). In addition to the expression of regular plasma cell antigens, CD38 and PCA-1, CD45 was found on both fresh cells and KHM-11. Other T-or B-cell antigens, such as CD2,4,8,19 and 20 were negative. IL-6 was found in the culture supernatant of KHM-11, and this supernatant stimulated the growth of this cell lines, indicating an IL-6 autocrine mechanism. These findings indicate that KHM-11 is a CD45-positive immature plasma cell line.Both cell lines, KHM-10B and KHM-11 should be a useful tool for understanding the pathogenesis of B cell maliganancies.